Muscle 1 Flashcards
Name the three types of muscle
Skeletal -movement (voluntary) -respiration (involuntary) -whole body metabolism-> largest metabolic organ in the body -it's striated and multi uncleared; the nuclei are peripheral -controlled by motor end plate Cardiac -pumping blood to lungs and body -striated and mostly mononucleated -Controlled by intercalated discs Smooth -peristalsis -vascular tone -not striated and has central nuclei -multiple levels of control
What is the anatomical organization of skeletal muscle?
Muscle->fascicle -> myofiber/muscle fiber ->myofibril -> sacromere -> myofilament
Each muscle cell has its own blood supply
Sacromere share made up of myofilaments
Define myofiber or fiber
A single muscle cell
Define myofibril
Rod-like series of sarcomeres
Define sarcomere
Basic contractile unit of the cell, contains the myofilaments
Define myofilament
Thick and thin filaments of a sarcomere
Define sarcoplasm
Cytoplasm of muscle cells
Define the sarcomere and its components
The sarcomere is the basic contractile unit of the muscle cell.
Spans from z disc to z disc and on either side there is an I band and next to that is the A bands
The M line splits the sarcomere in half and is made up of mainly thick filaments
The H zone is made up of thick filament proteins solely
A bands have both think and thick filaments. It’s the site of cross bridge reactions
I bands have on thick filament and the rest is thin filament
Z disc: thin filament version of the M line, mechanically sensitive, contain thin filament molecules as well as signaling molecules and structural proteins
Describe thick filament
Spans from a band to a band with the exception of Titin
Titin- molecular “spring”
-the largest protein know to man
-spans Z disc to M-line and back again
-structural support for the entire sarcomere
-sets passive tension
Myosin-molecular “motor”
-two pairs of light chains and one pair of heavy chains
-contains the catty tic subunit that participates in the creation of the cross-bridges
Describe the thin filament
Can be found A band to A band Provides a lot of control over contraction Provides the docking site of myosin which is actin I band is exclusively, with the exception of titin, made out of thin filament proteins Actin -the molecular rope Tropomyosin -coiled coil, inhibitory protein -regulated by troponin Troponin -Troponin C: Ca 2+ binding -Troponin I: Inhibitory -Troponin T: Tropomyosin binding
Thin and Thick Filaments interact explain how this involves calcium concentrations.
Contraction occurs from the interaction of Thick and thin filaments
Low sarcoplasma Ca2+ Concentration
-the probability of calcium binding is lower than at higher calcium concentration
-at low or no concentration calcium in the sarcoplasma, there is a steric blocking of Tropomyosin near the cross bridge
High sarcoplasma Ca2+ Concentration
-at high sarcoplasmic concentrations we see a conformational change in the thin filament regulatory proteins
What is lattice spacing?
Muscle fibers are not fat
Cross sections of the sarcomere at various regions reveal various hexagonal spatial distribution of sarcomere proteins
Hexagonal organization of thin and thick filaments
What is the sliding filament theory of contraction?
During relaxation, the H- zones andI bands are at max width, and the actin and myosin filaments lie parallel to each other. As contractions begins, the actin filaments are pulled toward the m-line, in this way the actin filaments “slide” over the thick filaments to a point in the fully contracted muscle where the ends of the thin filaments overlap. THe H-zone disappears in a fully contracted muscle and the I band becomes very narrow.
What does omecamtiv mecarbil do?
Increases the entry rate of myosin into the tightly bound, force producing state with actin
What are the steps of action potential?
1) action potential is propagated down an axon
2) this action potential triggers the opening of voltage gated Ca2+ channels
3) increase in cytosolic Ca2+ concentration in the pre-synaptic axon terminal rises, triggering release of a NT
4) acetylcholine floods the synaptic space, where it binds to receptors
5) the acetylcholine receptors allow the influx of sodium and the effluent of potassium
6) this causes a localized, rapid depolarization of the post synaptic cell which we can call an end plate potential
7) degradation of NT removes the signal
